1. Field of the Present Invention
The present invention relates to a DNA-binding protein YB-1-containing collagen accumulation inhibitor.
2. Description of the Related Art
In cases of diseases and abnormalities such as liver cirrhosis, interstitial pulmonary disease, chronic renal insufficiency (or a disease leading to a chronic renal insufficiency), post-inflammatory hyperplastic scar, postoperative scar or burn scar, or scleroderma, arteriosclerosis, hypertension, rheumatoid arthritis and the like, an excessive integration of a extracellular matrix such as a collagen leads to a fibrotic and hard tissue, resulting in a dysfunction of an organ or tissue as well as a scar formation. Such excessive integration of an extracellular matrix is induced by an impaired balance between the biosynthesis and the degradation of a collagen which leads to an excessive production. In fact, it was observed that a tissue once in a fibrotic state underwent an increased expression of a collagen gene, especially of a type-I collagen gene [J. Invest. Dermatol., 94, 365, (1990), Proc. Natl. Acad. Sci. USA, 88, 6642 (1991)]. Also in various animal models of fibroses, a treatment with interferon gamma reduces the expression of a type-I collagen gene in a tissue, resulting in a reduced amount of the collagen, which leads to a recovery from a fibrotic state of the tissue [Exp. Lung Res., 21, 791-808, (1995), Kidney Int., 47, 62-69, (1995), J. Hepatol., 28, 471-479 (1998), J. Hepatol., 26, 894-903 (1997)]. It was also reported that the level of TGFβ, which is one of cytokines, was increased in a tissue once in a fibrotic state [J. Invest. Dermatol., 94, 365 (1990), Proc. Natl. Acad. Sci. USA, 88, 6642 (1991)]. TGFβ was also reported to increase the expression of a type-I collagen gene and to be involved in an excessive production of the collagen, thus also in the conversion of a tissue into a fibrotic state [Lab. Invest., 63, 171, (1990), J. Invest. Dermatol., 94, 365 (1990)].